中药肠炎康对溃疡性结肠炎大鼠免疫功能的影响

Effect of Chang Yan Kang on Immunologic Function of Rats with Ulcerative Colitis

目的 :探讨溃疡性结肠炎 ( UC)发病过程中的免疫异常机制及中药肠炎康 ( CYK)口服液对本病的治疗机理。方法 :通过免疫方法成功复制 UC大鼠模型 ,应用 CYK口服液及对照药物柳氮磺胺吡啶 ( SASP)分别灌胃治疗 5 0 d,观察并分析治疗前后脾细胞 Con A刺激指数、LPS刺激指数、IL- 2、IFN- r水平及 NKc杀伤活性变化。结果 :模型组大鼠脾细胞 Con A刺激指数、NKc杀伤活性明显下降 ( P<0 .0 1 ) ,IL- 2、IFN- r水平也有下降 ( P<0 .0 5 ) ;而脾细胞 LPS刺激指数明显升高( P<0 .0 5 )。治疗后 ,CYK组大鼠脾细胞 Con A刺激指数、IL- 2、IFN- r水平及 NKc杀伤活性同模型组比较均有明显提高 ;但脾细胞 LPS刺激指数同模型组比较差异无显著性 ( P>0 .0 5 )。SASP组大鼠脾细胞 LPS刺激指数同模型组比较明显下降 ( P<0 .0 5 ) ;其 IL- 2、IFN- r水平及 NKc杀伤活性同模型组比较差异无显著性 ( P>0 .0 5 )。结论 :溃疡性结肠炎大鼠细胞免疫功能减退 ,体液免疫增强。CYK能促进 UC大鼠肠粘膜溃疡修复及炎症消退 ,在恢复其细胞免疫功能方面 ,优于 SASP,但对 UC大鼠体液免疫的抑制作用不及 SASP。

Objective:To study the immunologic mechanism of ulcerative colitis (UC) and the treatment mechanism of Chang Yan Kang (CYK). Methods:The UC rat models are reproduced successfully by immune method. CYK and Salicylazosulfapyridine (SASP) were applied to the models for 50 days. Some changes before and after treatment including the levels of spleen cell ConA SI,LPS SI,IL 2,IFN r, NKc killing activating in model rats were analyzed. Results:Compared with normal group, spleen cell Con SI, NKc killing activity ( P <0.01) and IL 2,IFN r level decreased significantly in model group ( P <0.05) and spleen cell LPS SI increased ( P <0.05). Spleen cell ConA SI, IL 2,IFN r level and NKc killing activity after treatment increased significantly in CYK group, but no significant difference in spleen cell LPS SI compared with model group ( P >0.05). Spleen cell LPS SI( P <0.05) decreased significantly in SASP group and spleen cell ConA increased ( P <0.05),but which was lower than that in CYK group( P <0.05).There was no significant difference in IL 2,IFN r level and NKc killing activity ( P <0.05) compared with model group, which was lower than normal group ( P <0.05). Conclusion:The results show a decrease in cellular immunity, NKc killing activity and increase in humoral immunity of UC rats. CYK can help the restoration of colonic mucosa of UC rats and disappearance of inflammation. It is superior to SASP in increasing NKc killing activity and restoring the cellular immunity of UC rats, but less effective in inhibiting humoral immunity in UC rats.